A gene restores ageing myelin repair cells in mice
As the brain ages, it becomes less able to repair myelin, the protective sheath around nerve fibres. Researchers have now identified a gene that significantly restores this capacity in aged mice.
Myelin is produced by specialised brain cells called oligodendrocytes, which develop from precursor cells (oligodendrocyte progenitor cells, or OPCs). In young animals, OPCs readily mature into fully functional myelin-producing cells. In older animals, this process slows considerably, impairing recovery after injury and reducing the brain’s capacity for adaptive learning through new myelin connections.
A computational pipeline identifies the switch
The research team developed a computational tool called gSWITCH to track gene activity patterns as cells develop over time. By comparing young and aged OPCs, the tool identified genes whose regulation changes with age. Several candidates emerged. The transcription factor Bcl11a stood out as a potential master regulator of multiple age-related changes.
The study, published in eLife, showed that blocking Bcl11a reduced OPC differentiation into oligodendrocytes. Overexpressing the gene in aged OPCs significantly enhanced their ability to mature. In aged mice with experimentally induced myelin damage in the spinal cord, Bcl11a overexpression increased the number of newly differentiated cells within the lesion.
An evolutionarily conserved gene
The researchers also found that Bcl11a’s amino acid sequence has remained highly stable throughout vertebrate evolution, a sign that the gene is under strong evolutionary pressure to preserve its function. This suggests it plays a fundamental biological role.
These findings come from mice. Whether the same approach would work safely in humans remains to be tested. The researchers describe the results as a starting point for exploring repair strategies in conditions where myelin damage plays a role.
Search terms to explore further: oligodendrocyte progenitor cell ageing differentiation, remyelination transcription factors, age-related myelin degeneration treatment